Herpesviridae family double-stranded DNA virus

i, ps
most common cause of congenital viral
infection

the most common ophthalmic manifestation of

CMV retinitis both congenital CMV infection and of CMV as
an opportunistic infection

leukemia

lymphoma

kh Ma
D
rhegmatogenous retinal detachments with
immunocompetent adults in contrast to CMV retinitis before introduction of combination 30% of patients with HIV/AIDS developed
multiple breaks developed in 33% per eye per
antiretroviral therapy CMV retinitis
year
chronic or recurrent unilateral anterior uveitis
80% decline in new cases/year of CMV
retinitis
ocular hypertension Introduction

fail combination antiretroviral treatment

M
similar to VZV corneal edema associated with
combination antiretroviral regimens
new cases of CMV retinitis continue to occur abandon treatment
causes illness in immunocompromised
variable degrees of sectoral iris atrophy HIV/AIDS among patients who
patients
CMV anterior uveitis experience immune reconstitution but do not
demonstration of CMV DNA by PCR analysis develop CMV-specific immunity

intraocular antibodies directed against CMV by CMV retinitis confers a twofold increased risk
diagnosis in mortality among patients with a CD4+ T-cell
enzyme-linked immunosorbent assay (ELISA)

ye d
count <100 cells/µL

negative study results for HSV and VZV

resistant CMV infection in patients with CMV
retinitis is further associated with increased
specific, prolonged, systemic anti-CMV mortality
valganciclovir
treatment

ha in
treatment
transplant recipients
relapses are common after discontinuation of therapy
systemic immunomodulation

fever
infects retinal vascular endothelial cells crosses the blood–ocular barrier cell-to-cell transmission within the retina
Pathogenesis virus reaches the eye hematogenously
thrombocytopenia

as M
associated with other systemic manifestations
anemia
of disseminated disease small, white retinal infiltrate masquerading as
early retinitis inevitable progression without treatment
a cotton-wool spot
pneumonitis

hepatosplenomegaly

11%-22% prevalence

associated systemic disease findings

M gy
clinical fundus appearance classic or fulminant retinitis
large areas of retinal hemorrhage against a
background of whitened, edematous, or
evidence of viral inclusion bodies or positive diagnosis of congenital disease Congenital CMV retinitis necrotic retina Figure 7-7 (© 2020 American Academy of
PCR in urine, saliva, and subretinal fluid
Ophthalmology)
of value 5–24 months after the loss of the
complement-fixation test
maternal antibodies posterior pole, from the disc to the vascular
arcades, in the distribution of the nerve fiber
resolution of the retinitis leaves both layer
pigmented and atrophic lesions 9.7.4. Infectious Ocular
Inflammatory Diseases (IV): associated with blood vessels
children with congenital CMV infection should
Cytomegalovirus (CMV)
o be monitored at regular intervals for potential
ocular involvement later into childhood

≤1/3
CMV retinitis can occur later in life

retinal detachment
clinical presentation 3 distinct variants
retinal periphery
an ol
optic atrophy complications

little or no retinal edema, hemorrhage, or

cataract granular or indolent form vascular sheathing

Intravenous acyclovir for HSV & VZV antiretroviral therapy

Figure 7-8 (© 2020 American Academy of
Ophthalmology)
ganciclovir (5 mg/kg twice daily)
m lm

effective against CMV and also HSV-1 & active retinitis progressing from the borders of
HSV-2 foscarnet (90 mg/kg twice daily) high-dose intravenous induction
the lesion

x2 weeks

may require only 6 months of anti-CMV

antiretroviral therapy–naive patients
therapy

may require long-term maintenance therapy antiretroviral therapy–experienced patients variant of “frosted-branch” angiitis, an
perivascular form idiopathic retinal perivasculitis initially
described in immunocompetent children
Ar ha

low-dose oral maintenance therapy

monitor at 3-month intervals
remain at risk for recurrence
(CD4+ T lymphocytes ≥100 cells/µL x 3–6
months)
patients on antiretroviral therapy with
sustained immune recovery Figure 7-9 (© 2020 American Academy of
systemic anti-CMV maintenance therapy may effective against CMV Ophthalmology)
be safely discontinued
Management
anti-CMV therapy
followed by maintenance therapy (900 mg/
x3 weeks oral valganciclovir (900 mg twice daily) diagnosis of CMV retinitis in patients with HIV/
day)
AIDS or undergoing IMT is essentially clinical

highly effective in treating intraocular disease

high sensitivity and specificity
Diagnostic tests
immunocompromised patients with atypical
t

particularly effective for patients with vision- lesions or whose disease is not responding to PCR (aqueous or vitreous) to differentiate CMV from other herpetic
threatening posteriorly located retinitis anti-CMV therapy causes of necrotizing retinitis and from
toxoplasmic retinochoroiditis
ph

useful alternative in patients who cannot intravitreal injection of ganciclovir or foscarnet

tolerate intravenous systemic therapy
(myelotoxicity)

intravitreal injection + oral valganciclovir may leaves extraocular systemic CMV and the
obviate this limitation fellow eye untreated

full-thickness, coagulative necrotizing retinitis

aggressive anti-CMV therapy initiated at the
same time as antiretroviral treatment may
decrease the incidence of immune recovery
uveitis
Figure 7-10 (© 2020 American Academy of Ophthalmology)
O

secondary diffuse choroiditis

Pathology

large eosinophilic intranuclear inclusions

infected retinal cells show pathognomonic small, multiple, basophilic cytoplasmic

cytomegalic changes inclusions

viral inclusions may be present in RPE and

vascular endothelium

viral particles with the typical morphology of

electron microscopy
the herpes family

Ophthalmology Mind Maps/Arman Mashayekhi, MD